VDR and tuberculosis: In 2006, Liu and colleagues showed that the triggering of toll-like receptors (TLRs) on the cell surface of human macrophages by tuberculosis protein caused the upregulation of genes leading to the production of the vitamin D receptor (VDR), a polymorphic nuclear receptor that regulates the expression of genes crucial for immune function and involved in cytokine production and the vitamin D-1-α-hydroxylase enzyme, leading to both increased levels of active vitamin D and increased potential binding of calcitriol with the VDR [11].